Effect of Gypenosides on TGF-β_1/Smad Signal Pathway in Rats with Liver Fibrosis Induced by Carbon Tetrachloride

Objective: To investigate the effect of gypenosides on TGF-β1/Smad signal pathway in rats with liver fibrosis induced by carbon tetrachloride(CCl4).Methods: The Wistar male rats were divided into normal group,model group,gypenosides group and colchicine group,and except the rats in normal group,the liver fibrosis model was induced by CCl4.The rats in gypenosides and colchicine groups were administrated with gypenosides(200 mg/kg.d) and colchicine(0.1 mg/kg.d) respectively and the other rats were administrated with sterile water from the seventh week,with a course of three weeks.The state of all the rats was observed,the content of hepatic hydroxyproline(Hyp) was tested,and the pathological changes of liver tissues were observed.In addition,the expressions of α-smooth muscle actin(α-SMA) and transforming growth factor-β1(TGF-β1),TGF-β1 receptor(TβR) Ⅰ,TβR-Ⅱ,Smad2/p-Smad2 and Smad3/p-Smad3 were examined.Results: Compared with the normal group,the content of Hyp of rats in model group was increased,the hepatic lobule was destroyed,and there were serious steatosis,inflammatory cell infiltration and much fibrosis in the liver;the expressions of α-SMA,TGF-β1,TβR-Ⅰ,TβR-Ⅱ,Smad2,p-Smad2 and p-Smad3 were significantly increased,while there was no statistical difference on Smad3 expression between model and normal group.Compared with model group,the content of Hyp of rats in gypenosides and colchicine groups was decreased,and the pathological changes of liver tissues were improved;the expressions of α-SMA,TGF-β1,Smad2,p-Smad2 and p-Smad3 of rats in gypenosides group were obviously decreased;the expressions of α-SMA,TGF-β1,Smad2 and p-Smad3 of rats in colchicine group were markedly decreased.Conclusion: The gypenosides can alleviate the liver fibrosis of rats induced by CCl4,and its mechanisms may have relationship with inhibiting the activation of hepatic stellate cell,the secretion of TGF-β1 and signal pathways of p-Smad2 and p-Smad3.